In masticating chewing gum, a large quantity of irritative saliva is secreted. For this reason, various studies have been done on the relation of chewing gum to dental caries and periodontal diseases.
Richardson et al, have reported that debris in saliva can be reduced by masticating gum. Shannon and Suzuki et al. have reported that by masticating gum secretion of whole saliva increases as does pH. Further, Volker reports that gum mastication depresses dental caries, gingival inflammation and accumulation of dental calculus.
Intermixed with diverse additives, gum is applied to prevention of dental caries and periocontal diseases. The effect, however, is not consistent. The reason for this is that the ingredients of the gum used by each researcher are diffarent, and therefore, it seems to be difficult to estimate results on the same basis.
In addition, the influence of constituents of secreted saliva produced by masticating gum is relevant.
However, there have been few reports dealing the constituents of saliva produced while masticating gum. To the author's knowledge, there also seem to be no reports on organic acid. For these reasons, the present study was concerned with organic acid detected in whole saliva and in parotid gland saliva. The study was carried out using widely available gums (peppermint and juicy) by means of High-Performanced liquid chromatography.
As a result of the study, the author arrived at the following conclusions:
1. Such organic acids as lactic acid, acetic acid, formic acid, malic acid, propionic acid, citric acid and succinic acid were detected in spontaneously flowing whole saliva and in whole saliva produced while masticating gum base. The organic acids mentioned above and n-butyric acid were detected in the whole saliva produced from peppermint gum mastication. Pyroglutamic acid and n-butylic acid were detected in the whole saliva from juicy gum mastication.
Acetic acid was the most prevalent organic acid detected in spontaneously flowing whole saliva and whole saliva produced while masticating gum base. Propionic acid, lactic acid, citric acid, scucinic acid, formic acid and malic acid followed in descending order. Acetic acid was the most common in whole saliva in masticating peppermint gum, while lactic acid, propionic acid, formic acid, malic acid, citric acid, succinic acid and n-butyric acid followed in descending order. Lactic acid was the most common in whole saliva in masticating juicy gum, while acetic acid, propionic acid, formic acid, succinic acid, citric acid, n-butyric acid, propionic acid, pyroglutamic acid and malic acid followed in descending order.
2. Such organic acid as lactic acid, aceticacid, formic acid, malic, acid propionic acid, citric acid and succinic acid were detected in spontaneously flowing parotid gland saliva parotid saliva produced while masticating gum base. In addition to the above acid, n-butyric acid was detected in parotid gland saliva in masticating peppermint gum and pyroglutamic acid and n-butyric acid were detected in parotid gland saliva in masticating juicy gum.
Lactic acid was the the mast prevalent in spontaneously flowing parotid gland saliva, while acetic acid, formic acid, citric acid, malic acid, propionic acid and succinic acid followed in descending order. Lactic acid was the mast prevalent in parotid gland saliva in masticating gum, while acetic acid, formic acid, citric acid, propionic acid, malic acid and succinic acid followed. Acetic acid was the most prevalent in parotid gland saliva in masticating peppermint gum, followed by lactic acid, formic acid, propionic acid, citric acid, malic acid, succinic acid and n-butyric acid. Lactic acid was the most prevalent in parotid gland saliva in masticating juicy gum, while acetic acid, propionic acid, formic acid, succinic acid, citric acid, pyroglutamic acid, malic acid and n-butyric acid followed.

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This histological study was undertaken to examine the process of collagen phagocytosis by fibroblasts in gingival connective tissue in experimental gingivitis. Both in vivo and in vitro studies were done by means of electron microscopy and histochemistry.
Gin-packs (No. 2) were ligated around the necks of 6|36/3 teeth from 0 to 30 days in an adult male Macaca irus monkey that was maintained on soft food and water. At 30 days, the Gin-pack removed from 6 teeth neck, and the monkey was given hard food for 3 days with the object of healing the gingivitis. Gingival biopsy specimens were taken at day 0 (3), day 9 (3), day 30 (6) and day 33 (6) and were studied at light microscopic and ultrastructural levels.
In attempt to demonstrate the phagocytic nature of intracytoplasmic vacuoles, monolayer cultures of human gingival fibroblasts were incubated with collagen fibers for 6 days and were observed with an electron microscope. Some sample were examined at the ultrastructural level for acid phosphatase activity.
The following results were obtained:
1) 3: There was no evidence of inflammatory changes. About 30% of the fibroblasts within the connective tissue contained banded collagen fibrils.
2) 3: A variety of inflammatory cells (neutrophils, lymphocytes and mast cells) were found. Fibroblasts were increased in number compared with those in 3. About 20% of the fibroblasts within the connective tissue cotained banded collagen fibrils.
3) 6: Another cell type, the plasma cells, was found. The number of fibroblasts was decreased and intracellular collagen fibrils were not observed. 6 fibroblasts and intracellular collagen fibrils were increased in number compared with those in 6
4) The vacuoles in fibroblasts containing collagen fibrils showed a positive acid phosphatase reaction. These results strongly suggest that the intracellular vacuoles are phagosomes and the phagocytosed collagen fibrils are digested by lysosomal enzymes.
The subjective data showing that the majority of collagenphagocytosing fibroblasts were resting rather than actively synthesizing cells indicates that the phagocytosis of collagen by fibroblasts occurred mostly in stabilized tissues. In all likelihood, the fibroblasts obtained at all time periods of the study are of the same origin and differ in response to their local environment.

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Whole saliva was collected from patients suffering from periodontal disease (diseased group) and from clinically healthy subjects (normal group), homogenized (homogenized with a Voltex mixer) and the homogenate separated by centrifugation (centrifuged at 3, 000rpm for 10 minutes). The activity and content of lysozyme in the homogenate, supernatant and precipitate were measured by a modified method of Kakizaki's turbidimetric assay and the enzyme immuno-assay method of Yuzuriha et al.. The relationships between these values and the clinical findings, such as the GI-score, the DI-score, the pocket depth and the bone loss score, were studied.
The following results were obtained:
1. In the precipitate, the activity and content of lysozyme were found to be 70-80% of those in the homogenate.
2. The activity of lysozyme in the homogenate and precipitate was most stable when measured by the turbidimetric method after 1.5% bovine serum albumin had been added to a 1/15M phosphate buffer having a 6.0 pH; however, the supernatant was not changed. Further the activity of lysozyme was inhibited by the addition of NaCl to the buffer.
3. Storage of the saliva at -20°C increased the activity of lysozyme in the precipitate and decreased it in the supernatant; however, in the homogenate it remained unchanged.
4. The addition of mucin to whole saliva slight increased the activity of lysozyme in the supernatant. The addition of plaque bacteria to whole saliva inhibited the activity of lysozyme in the homogenate by approximately 20%. The addition of human serum to whole saliva increased the activity of lysozyme in the supernatant approximately five fold.
5. The lysozyme content in the homogenate and precipitate from the diseased group as measured by the enzyme immuno-assay were statistically higher than that from the normal group (p<0.05).
6. No statistically significant correlation between all the measured values and the clinical findings could be found.

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Clinical evaluation of periodontal conditions was performed with 80 adults (50 patients with periodontal disease and 30 students in the School of Dentistry, aged 11 to 60). The assessment was conducted using P-M-A index, pocket depth, debris index, Supra-and subgingival calculus indices and age.
Significant positive correlations among the indices were observed except between the debris index and the pocket depth, the debris index and the supragingival calculus index, the debris index and the age, and between the P-M-A index and the age.
To eliminate an associated factor, a first order partial correlation coefficient was calculated. Partial correlations of the pocket depth with the P-M-A index, the subgingival calculus index and the age were significantly positive, respectively. Also, positive partial correlation was obtained between the supragingival calculus index and the subgingival calculus index, the age and the supragingival calculus index. It was found that several positive correlations between the clinical indices disappeared by calculation when the two indices, the pocket depth and the subgingival calculus index, were held fixed respectively.
For evaluation of periodontal disease in epidemiological study, importance of measuring pocket depth and subgingival calculus was discussed.

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The object of present investigation was to demonstrate the levels of secretory IgA in the human dental plaque scraped from buccal sulcus.
The dental plaques which were obstained from 50 volunteers of students with clinically health in Gifu College of Dentistry were smeared on slide glasses and observed by fluorescein staining with FITC-labeled goat antiserum to human secretory IgA. The quality of secretory IgA was categorized in three degrees (+++, ++ and +) based on wideness of specific fluorescence.
Byimmunopathological observation' diffuse pattern, fiblillar or granular pattern were odserved. Degree of +++ showed highest frequency in the plaque from molar and lowest in incisor.
From the results, the following conclusins were obtained:
1) The levels of secretory IgA were related with an excretory passage of the parotid glands.
2) The levels of secretory IgA were also related with occurence area of the gingivitis.

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Discrepancy in quantity of secretory IgA between buccal and lingual dental plaque was clarified by immunopathological study.
Extensive fuorescence which showed existence of secretory IgA was observed in dental plque obtained from superior buccal molar and inferior lingual incisor sulcus. However, it was indicated that gross volume of secretory IgA in each teeth was equable through arrangement of the tooth. The results gave suggestion that arrest to oral bacterial invasion into the periodontal tissue by secretory IgA was given uniformly against all of the teeth since the dental plaque from superior buccal molar and inferior lingu-al incisor sulcus retained it most extensively.

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We reported that bacteria in dental plaque were arrested to penetrate into periodontal tissue by secretory IgA coating to the bacteria. It was clarified wheather some bacteria were coated by non-specific secretory IgA or not by a indirect fluorescence antibody technique in this study.
Staphylococcus aureus, Fusobacterium nucleatum and Candida albicans showed intensive fluorescence on their cell walls. These fluorescence indicated that they possesed the function of binding to secretory IgA. Streptococcus mutans, Streptococcus sanguis, Actinomyces viscosus and Actinomyces naeslundii showed small granular and scattered fluorescence on their cell walls. It was suggested that their binding function were lower than above three species from this observation. Specific fluorescence was not demonstrated on Staphylococcus epidermidis and Treponema macrodentium.

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It is well known that the fibronctin composed of cell surface and plasma fibronectin plays a role of promoting cell proliferation and then regeneration of injured tissue by its biological function. We reported that the fibronectin localized in various components of human inflamed gingiva, and gave suggestion that the substance was correlated to local resistance factor to periodontal disease.
This study was made to clarify the formation of fibronection in L-cells which cultured under several conditions. While L-cells cultured under very poor condition which disappered during culture for five days were not demonstrated the fibronectin in their cytoplasm, others included groups which cultured under poor condition were observed the formation. The fluorescence was categorized into three groups of diffuse, granular, and fibrillar pattern.
From above, it was suggested that the fibroblasts in periodontal tissue with inflammatory destruction formed fibronectin, promoted to proliferate themselves, and then led to regeneration of the injured periodntal tissue.

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Effect of age on collagen synthesis, protein synthesis and the activities of prolyl hydroxylase, collagenase and cathepsin D in the rat gingiva was studied. Male wistar rats of 4, 11-12 and 56-64 weeks old were used as young, adult and old groups, respectively. The results are as follows:
1) collagn synthesis of gingiva markedly decreased with aging; the value was about one-third in adult group and about one-tenth in old group as compared with that of young group. Protein synthesis also decreased but the rate of the decrease was slight when compared with the rate of collagen synthesis.
2) A marked decrease in prolyl hydroxylase activity was also found; the activity changed almost parallel with the rate of collagen synthesis.
3) collagenase activity was about a half in adult group and one-fourth in old group as compared with the activity of young group. A significant decrease in cathepsin D activity was also found.
These results indicate that the turnover of collagen in the rat gingiva markedly decreases with aging.

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The purpose of this study is to investigate the relation between herpes simplex virus and periodontal disease.
We collected 180 samples from non-operated human saliva, and 32 samples from saliva with periodontal disease at pre-operation, one and 7 days after operation, and furthermore collected gingiva during operation.
And then, from these samples we isolated herpes simplex virus by inoculation on tissue cultures of GMK cells (African green monkey kidney cells).
The results obtained are as follows:
1. Only one strain of herpes simplex virus was isolated from 180 samples of human saliva collected at Hospital of Kanagawa Dental College.
2. Herpes simplex virus were isolated with high rate from 32 samples of saliva in operated group as compared with 180 samples of saliva in nonoperated group.
3. 4 strains of herpes simplex virus were isolated from 32 samples of human gingiva with periodontal disease.
4. Herpes simplex virus isolated were determined as type 1 by plaque forming ability on CE (chick embryo) cells.
5. Consequently, it is suggested that herpes simplex virus is involved in periodontal disease.

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The purpose of this study was to measure the thickness of free and attached gingiva, alveolar mucosa and alveolar bone by the ultrasonic wave system.
Ten subjects with the healthy gingiva and alveolar mucosa were used in this study. The 18 points of the facial side on the maxillary anterior region of each subject were measured with ultrasonic wave. The thickness of alveolar bone was also measured in 3 subjects with periodontitis.
The results were as follows.
1. The free gingival thickness averaged 0.93mm±0.17, attached gingival thickness averaged 1.03mm±0.19 and alveolar mucosal thickness averaged 0.88mm±0.18.
2. The statistically significant correlation was found between the free gingival thickness and the attached gingival thickness, between the attached gingival thickness and the alveolar mucosal thickness.
3. The free and attached gingiva on the central incisors showed the highest thickness.
4. The thickness of alveolar mucosa on the lateral incisors were the highest.
5. The thichness of alveolar bone on the anterior teeth varied between 0.55mm to 1.0mm.

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The purpose of this study was to establish a method for detection of the gingival inflammation by measuring the capacitance of the gingival fluid.
Eight periodontally healthy students were selected for measuring the capacitance during development of the experimental gingivitis and eight patients with periodontal disease were selected for investigating the relationship between the degree of the disease and the capacitance.
Before measuring, the gingival area was washed and dried carefully. The sensor was inserted in the periodontal pocket and measured the capacitance for ten sec.
The correlation between the clinical findings and the capacitance of the gingival fluid was as follows.
1. Experimental gingivitis group
1) The capacitance of the gingival fluid tend to increase during the period. (p<0.01)
2) The significant correlation was found between the capacitance and Plaque Index, Gingival Index and Gingival Bleeding Index. (p<0.01)
2. Periodontal disease group
1) The significant correlation was found between the capacitance and Gingival Index and Gingival Bleeding Index. (p<0.01)
2) Less significant correlation was found between the capacitance and Plaque Index. (p<0.05)
3) Any significant correlation was not found between the capacitance and probing depth.

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The purpose of this study was undertaken to diagnostic and prognostic examination in the clinical routine procedures.
The thermistor probe (digital mutti-themistor 2752, Yokokawa Co, Ltd) was used for the measurment of gingival sulcus tempreature.
The 17 out paitientes were selected, and following parameters were recorded, in sequence, gingival index, plaque index, gingival bleeding index and probing depth.
The tempreature was measured at the center of facial and lingual postion in the first molar and incisor.
The correlation between gingival sulcus tempreature and plaque index was showed no signficant difference.
That tendency also showed on the gingival index and probing depth, but the correlation between the gingival sulcus temperature and gingivl bleeding index showed a significant difference. (p<0.01)

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The effectiveness against periodontal disease of a dentifrice containing dl-α-tocopheryl nicotinate (V dentifrice) was tested comparing with placebo (P dentifrice) for 4 weeks.
Subjects were 165 students of Josai Dental University who had no serious oral disease.
This study was conducted with double blind method.
The results were summarized as follows.
1) Subjects available for statistical analysis were 67 in each group. Subjects unavailable for statistical analysis were 16 in V dentifrice group and 15 in P detifrice group.
2) V dentifrice was significantly superior to P dentifrice in improvement of PMA index (p<0.01) and redness (p<0.01). On the other hand, there was no significant difference in improvement of dental plaque and swelling between two groups.
3) After 4 weeks of the study, reduction rate of Vdentifrice group and P dentifrice group were 40.6% and 27.1% in PMA index, 17.0% and 9.1% in redness, 13.7% and 5.9% in swelling, and 4.5% and 4.7% in dental plaque, respectively.
4) V dentifrice was significantly superior in general improvement to P dentifrice (p<0.01).
The percentage of generally improved subjects of V dentifrice group and P dentifrice group were 77.6% and 56.7%, respectively.
5) No particular side effect was obserbed throughout the study.

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The clinical effect of an S 30 dentifrice, containing a hypertonic salt, on simple gingivitis and marginal periodontitis was examined, using the double blind method, with an inactive placebo as the control. The S 30 dentifrice contains 30% sodium chloride, 0.05% isopropyl methylphenol, 0.01% thymol and 0.1% clove oil in a toothpaste base. Using the Scrubbing or Bass method, tooth brushing was performed by all the patients three times a day for 4 weeks.
The clinical effect of the S 30 dentifrice was assessed using the Mann-Whitney U-test based on the reduction ratio of the total scores of the indices to 4 clinical assessments (gingival redness, swelling, bleeding and pus-discharge) and the total number of the clinical conditions to 9 clinical assessments (plaque, calculus, redness, swelling, pocket depth, bleeding, pus-discharge, mobility and halitosis) respectively in an initial examination before using the S30 dentifrice was initiated and at the end of every weeks thereafter for the entire 4 weeks of the evaluation.
The results were as follows:
1. Simple gingivitis showed a statistically significant difference (P<0.01 and/or P<0.05), in the reduction ratio between the S 30 dentifrice and the placebo on the total scores and number of both the 4 clinical assessments after 2 and 3 weeks and the 9 clinical assessments after 1, 2 and 3 weeks, respectively.
2. Marginal periodontitis showed no significant difference in the reduction ratio between the S 30 dentifrice and the placebo on the total scores of the 4 clinical assessments: however, after 3 weeks, showed a significant difference (P<0.05), on the total number of the 9 clinical assessments.
3. Periodontal disease (gingivitis and periodontitis) showed a significant difference (P<0.01 and/or P<0.05), in the reduction ratio between the S 30 dentifrice and placebo on the total scores of the 4 clinical assessments after 3 weeks, and on the total number of the 4 clinical assessments after 1, 2 and 3 weeks, and on the total scores of the 9 clinical assessments after 2 and 3 weeks and on the total number of the 9 clinical assessments after 1, 2, 3 and 4 weeks, respectively.
4. The side effects were slight in 3 patients using the S 30 dentifrice and in 1 patient using the placebo.

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